Shock Response Research Articles

Seismic behavior of base isolated precast frame

The performance of the base-isolated precast frame is examined for both near-field and far-field earthquakes. For comparison, the corresponding base isolated monolithic frame is analyzed. The frames are isolated using a friction pendulum system (FPS), which is appropriately designed to take up the vertical load coming on the frames. The same isolators are provided for the monolithic and precast frames. Two types of precast frames are considered, namely frames with emulated and non-emulated connections. An ensemble of 7 different earthquakes is used for each type of earthquake to obtain the average responses, which include maximum base shear, maximum acceleration, maximum top story displacement, and maximum inter-story drift ratio (MIDR). SAP2000 is used for the non-linear time history analysis of the frames for different earthquakes. The studies are made for three levels of PGA, namely 0.4 g, 0.6 g, and 0.8 g. The study shows that a significant reduction in base shear, top story displacement and MIDR is achieved by base isolating the precast frames. However, the corresponding base isolated monolithic frame offers more reductions in response especially for MIDR. Of the two types of precast frames, the one with emulated connection shows marginally higher reductions of response as compared to the non-emulated connection. Further, the percentage reductions in responses in main shock and after shock remain almost the same for all cases.

Smart composite structural insulated panels (CSIPs) with embedded piezoelectric sensors for damage localization

Coastal communities face increasing vulnerability to natural disasters, necessitating resilient construction solutions. This study presents the development of smart composite structural insulated panels (CSIPs) embedded with piezoelectric sensors for damage localization in hurricane and tornado-prone areas. Experimental studies, such as four-point bending and in-panel compression tests, were conducted to analyse the shock response and failure modes of these smart CSIPs. Material characterization informs the development of finite element models for simulation, enhancing structural design. By integrating structural health monitoring capabilities, these smart CSIPs enable continuous tracking of their response to environmental factors, improving longevity and durability. Shock identification and localization in smart CSIPs are successfully demonstrated through numerical simulations and experimental validation, showcasing the potential step towards self-resilient structures in coastal regions. This novel approach provides real-time information on structural integrity, paving the way for improved safety and predictive maintenance of buildings and infrastructure utilizing CSIPs.

Proteostasis and Its Role in Disease Development.

Proteostasis (protein homeostasis) refers to the general biological process that maintains the proper balance between the synthesis of proteins, their folding, trafficking, and degradation. It ensures proteins are functional, locally distributed, and appropriately folded inside cells. Genetic information enclosed in mRNA is translated into proteins. To ensure newly synthesized proteins take on the exact three-dimensional conformation, molecular chaperones assist in proper folding. Misfolded proteins can be refolded or targeted for elimination to stop aggregation. Cells utilize different degradation pathways, for instance, the ubiquitin-proteasome system, the autophagy-lysosome pathway, and the unfolded protein response, to degrade unwanted or damaged proteins. Quality control systems of the cell monitor the folding of proteins. These checkpoint mechanisms are aimed at degrading or refolding misfolded or damaged proteins. Under stress response pathways, such as heat shock response and unfolded protein response, which are triggered under conditions that perturb proteostasis, the capacity for folding is increased, and degradation pathways are activated to help cells handle stressful conditions. The deregulation of proteostasis is implicated in a variety of illnesses, comprising cancer, metabolic diseases, cardiovascular diseases, and neurological disorders. Therapeutic strategies with a deeper insight into the mechanism of proteostasis are crucial for the treatment of illnesses linked with proteostasis and to support cellular health. Thus, proteostasis is required not only for the maintenance of cellular homeostasis and function but also for proper protein function and prevention of injurious protein aggregation. In this review, we have covered the concept of proteostasis, its mechanism, and how disruptions to it can result in a number of disorders.

Brain-derived neurotrophic factor in older adults exposed to simulated indoor overheating.

Brain-derived neurotrophic factor (BDNF) is a neuroprotective growth factor that increases in young adults during short, intense bouts of passive heat stress. However, this may not reflect the response in heat-vulnerable populations exposed to air temperatures more consistent with indoor overheating during hot weather and heatwaves, especially as the BDNF response to acute stressors may diminish with increasing age.We therefore evaluated the ambient and body temperature-dependent responses of BDNF inolder adults during daylong passive heating. Sixteenolder adults (6 females; aged 66-78years) completed 8-h exposure to four randomized ambient conditions simulating those experienced indoors during hot weather and heatwaves in continental climates: 22°C (air-conditioning; control), 26°C (health-agency-recommended indoor temperature limit), 31°C, and 36°C (non-airconditioned home); all 45% relative humidity. To further investigate upstream mechanisms of BDNF regulation during thermal strain, we also explored associations between BDNF and circulating heat shock protein 70 (HSP70; taken as an indicator of the heat shock response). Circulating BDNF was elevated by ~ 28% (1139 [95%CI: 166, 2112] pg/mL) at end-exposure in the 36°C compared to the 22°C control condition (P = 0.026; 26°C-and 31°C-22°C differences: P ≥ 0.090), increasing 90 [22, 158] pg/mL per 1°C rise in ambient temperature (linear trend: P = 0.011). BDNF was also positively correlated with mean body temperatures (P = 0.013), which increased 0.12 [0.10, 0.13]°C per 1°C rise in ambient temperature (P < 0.001). By contrast, serum HSP70 did not change across conditions (P ≥ 0.156), nor was it associated with BDNF (P = 0.376). Our findings demonstrate a progressive increase in circulating BDNF during indoor overheating in older adults.

The heat shock response of plants: new insights into modes of perception and signaling and how hormones contribute.

Plants have evolved specific temperature preferences, and shifts above this range cause heat stress with detrimental effects such as physiological disruptions, metabolic imbalances, and growth arrest. To reduce damage, plants utilize the heat shock response (HSR), signaling cascades that activate the heat shock factors (HSFs), transcription factors that control the heat stress-responsive transcriptome for activation of protective measures. While the core HSR is well-studied, we still know relatively little about heat stress perception and signal integration or cross-talk with other pathways. In the last few years, however, significant progress has been made in this area, which is summarized here. It has emerged that the plant hormones brassinosteroids (BRs) and abscisic acid (ABA) contribute to heat stress tolerance by impacting HSF modes of activity. Also, we began to understand that heat stress is sensed in different cellular compartments and that events in the nucleus, such as nuclear condensate formation via liquid-liquid phase separation, play a key role. In the future, it will be important to explore how these multilayered perception and signaling modes are utilized to understand how environmental context and developmental stage determine the outcome of heat stress effects on plant growth and development.

On the role of the retained porosity on the shock response of additively manufactured high-performance steel: Experiments, constitutive model and finite-element predictions

Experiments have shown that for quasi-static and moderate strain-rates (of the order of 102–103/s) the mechanical response of additively manufactured (AM) and traditionally processed high-strength steels is similar whereas the impact behavior is markedly different. In this paper, we reveal that the main reason for this difference is the retained porosity in the AM material. Fully-implicit finite element calculations are presented in which we simulate both the launching of the impact plate and the impact between the two plates. The constitutive model used is the elastic/plastic model for porous ductile materials with matrix displaying tension-compression asymmetry and Johnson-Cook hardening law that accounts for both strain-rate effects and plastic history. It is shown that even a very small initial porosity changes the wave front, decreases the Hugoniot while increasing the shock rise time, when compared to a void free material. Furthermore, quantitative comparisons between simulation results and plate impact data for both the AM and the wrought AF9628 steel are provided. The good agreement show that the model captures the impact response and illustrates the model capabilities to provide information on field variables that cannot be directly measured.Additive manufacturing (AM) of metals is rapidly advancing as a robust method for production of geometrically complex parts. To enhance understanding of material performance and open up additional application opportunities, dynamic characterization of newly printed alloys is required to validate their effectiveness. In this paper, we present results from plate impact testing of AF9628 steel, a newly developed high-strength low alloy martensitic steel for structural applications which require resistance to high-rate deformation. We put into evidence differences in the shock structure between the AM and the traditionally processed material. To gain understanding, we conduct fully-implicit finite element (FE) calculations in which we model both the launching of the impact plate and the impact between the two plates, respectively. An elastic/plastic damage model that accounts for the effects of the tension-compression asymmetry in plastic deformation and its influence on porosity evolution is used. The FE results reveal that even a very small amount of initial porosity leads to an increase in the shock rise time, explaining the observed trends. Furthermore, quantitative comparisons between simulation results and plate impact data for both the AM and the wrought AF9628 are provided. The good agreement show that the model captures the impact response and illustrates the model capabilities to provide information on field variables that cannot be directly measured.

Heat Shock Factor 1 forms nuclear condensates and restructures the yeast genome before activating target genes

In insects and mammals, 3D genome topology has been linked to transcriptional states yet whether this link holds for other eukaryotes is unclear. Using both ligation proximity and fluorescence microscopy assays, we show that in Saccharomyces cerevisiae, Heat Shock Response (HSR) genes dispersed across multiple chromosomes and under the control of Heat Shock Factor (Hsf1) rapidly reposition in cells exposed to acute ethanol stress and engage in concerted, Hsf1-dependent intergenic interactions. Accompanying 3D genome reconfiguration is equally rapid formation of Hsf1-containing condensates. However, in contrast to the transience of Hsf1-driven intergenic interactions that peak within 10–20 min and dissipate within 1 hr in the presence of 8.5% (v/v) ethanol, transcriptional condensates are stably maintained for hours. Moreover, under the same conditions, Pol II occupancy of HSR genes, chromatin remodeling, and RNA expression are detectable only later in the response and peak much later (&gt;1 hr). This contrasts with the coordinate response of HSR genes to thermal stress (39°C) where Pol II occupancy, transcription, histone eviction, intergenic interactions, and formation of Hsf1 condensates are all rapid yet transient (peak within 2.5–10 min and dissipate within 1 hr). Therefore, Hsf1 forms condensates, restructures the genome and transcriptionally activates HSR genes in response to both forms of proteotoxic stress but does so with strikingly different kinetics. In cells subjected to ethanol stress, Hsf1 forms condensates and repositions target genes before transcriptionally activating them.

Heat Shock Factor 1 forms nuclear condensates and restructures the yeast genome before activating target genes.

In insects and mammals, 3D genome topology has been linked to transcriptional states yet whether this link holds for other eukaryotes is unclear. Using both ligation proximity and fluorescence microscopy assays, we show that in Saccharomyces cerevisiae, Heat Shock Response (HSR) genes dispersed across multiple chromosomes and under the control of Heat Shock Factor (Hsf1) rapidly reposition in cells exposed to acute ethanol stress and engage in concerted, Hsf1-dependent intergenic interactions. Accompanying 3D genome reconfiguration is equally rapid formation of Hsf1-containing condensates. However, in contrast to the transience of Hsf1-driven intergenic interactions that peak within 10-20 min and dissipate within 1 hr in the presence of 8.5% (v/v) ethanol, transcriptional condensates are stably maintained for hours. Moreover, under the same conditions, Pol II occupancy of HSR genes, chromatin remodeling, and RNA expression are detectable only later in the response and peak much later (>1 hr). This contrasts with the coordinate response of HSR genes to thermal stress (39°C) where Pol II occupancy, transcription, histone eviction, intergenic interactions, and formation of Hsf1 condensates are all rapid yet transient (peak within 2.5-10 min and dissipate within 1 hr). Therefore, Hsf1 forms condensates, restructures the genome and transcriptionally activates HSR genes in response to both forms of proteotoxic stress but does so with strikingly different kinetics. In cells subjected to ethanol stress, Hsf1 forms condensates and repositions target genes before transcriptionally activating them.

Dynamic insights into thermal shock response of double-layer cylinders with FGM main layer and viscoelastic holder via generalized Green-Naghdi theory

This study investigates the dynamic thermoelastic response of a hollow cylinder composed of two distinct layers: a Functionally Graded Material (FGM) as the primary layer and an isotropic viscoelastic material as the supporting layer. Utilizing a power function, the material properties of the FGM layer are determined, while the viscoelastic layer follows the Kelvin-Voigt model. The research employs the generalized Green-Naghdi theory to formulate the heat transfer equation, capturing the energy dissipation and thermoelastic wave propagation within this novel configuration. Highly coupled equations governing both layers are derived, incorporating appropriate boundary and continuity conditions. The Chebyshev collocation element (CCE) method is utilized for the spatial solution, significantly reducing the computational effort by requiring only two higher-order elements. The Newmark time marching approach is employed to solve the resulting ordinary differential equations (ODEs). The model's accuracy is validated against existing literature, and parametric studies are conducted to evaluate the impact of thermal shock on the FGM layer. It has been observed that the presence of the viscoelastic barrier effectively impedes the full penetration of stress waves, thereby reducing the potential for shock-induced damage.

RiboTag RNA Sequencing Identifies Local Translation of HSP70 In Astrocyte Endfeet After Cerebral Ischemia.

Brain ischemia causes disruption in cerebral blood flow and blood-brain barrier (BBB) integrity which are normally maintained by the astrocyte endfeet. Emerging evidence points to dysregulation of the astrocyte translatome during ischemia, but its effects on the endfoot translatome are unknown. In this study, we aimed to investigate the early effects of ischemia on the astrocyte endfoot translatome in a rodent model of cerebral ischemia-reperfusion. To do so, we immunoprecipitated astrocyte-specific tagged ribosomes (RiboTag IP) from mechanically isolated brain microvessels. In mice subjected to middle cerebral artery occlusion and reperfusion and contralateral controls, we sequenced ribosome-bound RNAs from perivascular astrocyte endfeet and identified 205 genes that were differentially expressed in the translatome after ischemia. Pathways associated with the differential expressions included proteostasis, inflammation, cell cycle, and metabolism. Transcription factors whose targets were enriched amongst upregulated translating genes included HSF1, the master regulator of the heat shock response. The most highly upregulated genes in the translatome were HSF1-dependent Hspa1a and Hspa1b , which encode the inducible HSP70. We found that HSP70 is upregulated in astrocyte endfeet after ischemia, coinciding with an increase in ubiquitination across the proteome. These findings suggest a robust proteostasis response to proteotoxic stress in the endfoot translatome after ischemia. Modulating proteostasis in endfeet may be a strategy to preserve endfeet function and BBB integrity after ischemic stroke.

Rapid and Robust Identification of Sepsis Using SeptiCyte RAPID in a Heterogeneous Patient Population.

Background/Objective: SeptiCyte RAPID is a transcriptional host response assay that discriminates between sepsis and non-infectious systemic inflammation (SIRS) with a one-hour turnaround time. The overall performance of this test in a cohort of 419 patients has recently been described [Balk et al., J Clin Med 2024, 13, 1194]. In this study, we present the results from a detailed stratification analysis in which SeptiCyte RAPID performance was evaluated in the same cohort across patient groups and subgroups encompassing different demographics, comorbidities and disease, sources and types of pathogens, interventional treatments, and clinically defined phenotypes. The aims were to identify variables that might affect the ability of SeptiCyte RAPID to discriminate between sepsis and SIRS and to determine if any patient subgroups appeared to present a diagnostic challenge for the test. Methods: (1) Subgroup analysis, with subgroups defined by individual demographic or clinical variables, using conventional statistical comparison tests. (2) Principal component analysis and k-means clustering analysis to investigate phenotypic subgroups defined by unique combinations of demographic and clinical variables. Results: No significant differences in SeptiCyte RAPID performance were observed between most groups and subgroups. One notable exception involved an enhanced SeptiCyte RAPID performance for a phenotypic subgroup defined by a combination of clinical variables suggesting a septic shock response. Conclusions: We conclude that for this patient cohort, SeptiCyte RAPID performance was largely unaffected by key variables associated with heterogeneity in patients suspected of sepsis.

Influence of phase stability on postshock mechanical properties and microstructure evolution in Ti-17 alloy

There has been a growing surge of interest in examining the shock response of titanium alloys, owing to their considerable potential for military applications. The present study aims to reveal the influence of phase stability on the shock-induced mechanical response and substructure evolution of a metastable β titanium alloy, namely, Ti-17. This investigation included extensive work, such as plate impact tests, quasi-static reloading compression tests, and electron microscope analyses. The microstructural evaluations following the shock-wave loading unveil planar slip as the prevailing deformation mechanism in Ti-17 with a bimodal microstructure with stable α and β phases. However, when the shock stress exceeds 10 GPa, the activation of {101¯1}α nano-sized twins was observed, leading to improved reloading ductility. This implies a novel strategy to achieve excellent strength-plasticity compatibility in titanium alloys through appropriate shock-wave loading. Conversely, in Ti-17 with an equiaxed β microstructure, the metastability of the β phase leads to the activation of shock-induced α″ martensite, shock-induced ω, and planar slip. Two distinct forms of interaction involving the α″ laths, i.e., shear and truncation, were also observed. Phase stability greatly influences substructure evolution, which ultimately controls the reloading mechanical properties of the postshock Ti-17 alloy.

Investigation on the Effect of Energy Release Rate of Aluminized Explosive on the Damage of Underwater Targets

AbstractAs a type of high‐energy explosive, aluminized explosives are extensively used in underwater weapons and ammunition. This study aims to investigate the energy release rate on the damage of underwater targets caused by aluminized explosives (RDX/Al). The ship was selected as a target, and numerical simulations were conducted using AUTODYN software to study the energy release rate corresponding to different particle sizes of aluminum powder (25 nm −300 μm) in the underwater explosion process of RDX/Al, as well as its destructive effect on targets in the water. The research quantitatively evaluates the whole ship′s destruction results, including longitudinal bending deformations and crevasse. In addition, typical cabins were selected in this study to assess the local damage effects by analyzing stress, shock wave pressure, displacement, and acceleration shock response. Based on the damage results, it was revealed that RDX/Al with aluminum powder particle sizes ranging from 54 nm to 145 nm exhibited the most optimal damaging effects on ships after underwater explosions. These findings provide a basis for improving the destructive power of aluminized explosives against underwater targets, simultaneously, they can be utilized by ship designers to guide research and development of improved protective measures, aiming to reduce the vulnerability of ships to explosive attacks.

Hiding in plain sight: Optimizing topoisomerase IIα inhibitors into Hsp90β selective binders

Due to their impact on several oncogenic client proteins, the Hsp90 family of chaperones has been widely studied for the development of potential anticancer agents. Although several Hsp90 inhibitors have entered clinical trials, most were unsuccessful because they induced a heat shock response (HSR). This issue can be circumvented by using isoform-selective inhibitors, but the high similarity in the ATP-binding sites between the isoforms presents a challenge. Given that Hsp90 shares a conserved Bergerat fold with bacterial DNA gyrase B and human topoisomerase IIα, we repurposed our ATP-competitive inhibitors of these two proteins for Hsp90 inhibition. We virtually screened a library of in-house inhibitors and identified eleven hits for evaluation of Hsp90 binding. Among these, compound 11 displayed low micromolar affinity for Hsp90 and demonstrated a 12-fold selectivity for Hsp90β over its closest isoform, Hsp90α. Out of 29 prepared analogs, 16 showed a preference for Hsp90β over Hsp90α. Furthermore, eleven of these compounds inhibited the growth of several cancer cell lines in vitro. Notably, compound 24e reduced intracellular levels of Hsp90 client proteins in MCF-7 cells, leading to cell cycle arrest in the G0/G1 phase without inducing HSR. This inhibitor exhibited at least a 27-fold preference for Hsp90β and was selective against topoisomerase IIα, a panel of 22 representative protein kinases, and proved to be non-toxic in a zebrafish larvae toxicology model. Finally, molecular modeling, corroborated by STD NMR studies, and the binding of 24e to the S52A mutant of Hsp90α confirmed that the serine to alanine switch drives the selectivity between the two cytoplasmic isoforms.

Mapping the integration of climate considerations in social protection in LMICs: An assessment of ninety-eight climate-relevant social protection programs

Social protection can be an important policy tool to manage the socioeconomic impacts of climate change and climate risk, including poverty and inequality. Despite growing interest from policy makers and academics, a systematic effort document capture and analyze the current integration of climate considerations in social protection programs does not yet exist. This understanding is crucial for designing climate-relevant policies and programs that help more effectively manage climate change impacts.Our research systematically maps for the first time the integration of climate considerations in social protection programs in low- and middle-income countries (LMICs). Using a mixed-methods approach, we identify 98 climate-relevant social protection programs and collect data on over 70 variables related to their scope and climate relevance at policy, design, and implementation level. We seek to answer the question: to what extent and how are social protection programs in LMICs climate-relevant? for further research.Our findings reveal a significant number of long-standing climate-relevant social protection programs that reach large populations and involve substantial financial investments globally. At policy level, these programs often lack climate considerations, and a minority are primarily climate-focused by design. At the implementation level, most programs show climate-relevant actions or results, typically centered on shock response, though our findings suggest they have the potential to address broader climate functions. Overall, our results empirically substantiate long-held assumptions about climate-relevant social protection and highlight areas for further research. We also make the database openly available and encourage its use by policymakers and practitioners.

Effect of Mn element on shock response in CoCrFeNiMnx high entropy alloys

Abstract The effect of Mn element on shock response of CoCrFeNiMn x high entropy alloys (HEAs) are investigated using molecular dynamics simulations. Structural analysis shows that Mn-rich CoCrFeNiMn x HEA has a larger average atomic volume. The elastic properties of CoCrFeNiMn x HEAs under various hydrostatic pressures are studied, revealing that the elastic modulus decreases with increasing of Mn content. The shock thermodynamic parameters are quantitatively analyzed. The Mn-dependent shock Hugoniot relationship of CoCrFeNiMn x HEAs is obtained: U s = 1.25 + (5.21–0.011x)U p. At relatively high shock pressure, the increase in Mn content promotes the formation of clustered BCC structures and hinders the development of dislocations. In addition, more FCC structures in Mn-rich CoCrFeNiMn x HEAs transform into disordered structures during spallation. Spall strength decreases with increasing Mn content. This study can provide a reference for the design and application of CoCrFeNiMn HEAs under shock loading.

HSF1/HSP25 system protects mitochondria function from heat stress and assists steroidogenesis in MA-10 Leydig cells

Heat shock response is characterized by the induction of heat shock proteins (HSPs) or molecular chaperones that maintain protein homeostasis. Heat shock transcription factor 1 (HSF1) plays a central role in heat shock response in mammalian cells. To investigate the impact of the heat shock response mechanism on steroidogenesis, we generated MA-10 mouse Leydig tumor cells deficient in HSF1 using CRISPR-Cas9 genome editing. Under heat stress conditions, the levels of StAR protein, but not its mRNA, decreased more in HSF1-knockout cells than in wild-type cells, confirming that HSF1 stabilizes StAR protein. Simultaneously, HSP110, HSP70, and HSP25 were markedly upregulated in an manner dependent on HSF1. Mitochondrial membrane potential (MMP) and ATP synthesis were decreased in HSF1-knockout cells under heat stress conditions, and mitochondrial fragmentation was enhanced. Furthermore, treatment with carbonyl cyanide 3-chlorophenylhydrazone (CCCP), a disruptor of MMP, reduced the levels of StAR protein to a greater extent in HSF1-knockout cells than in wild-type cells, which was associated with decreased MMP and ATP synthesis. Unexpectedly, HSP25 expression was markedly increased in wild-type cells following CCCP treatment. HSP25 knockdown reduces MMP under heat stress conditions and decreases StAR protein levels and progesterone synthesis. HSP25 overexpression in HSF1KO cells restored StAR protein levels. These results show that the HSF1/HSP25 pathway protects mitochondrial function and maintains StAR synthesis.

Systemic and Ovarian Impacts of Heat Stress in the Porcine Model.

Heat stress (HS) in mammals results from an imbalance in heat accumulation and dissipation. Fertility impairments consequential to HS have been recognized for decades in production animals, and more recently, observations have been extended to other species including women. There are several systemic impacts of HS that can independently affect reproduction including metabolic endotoxemia, reduced plane of nutrition and endocrine disruption. At the level of the ovary, molecular pathways are altered by HS such as inflammation, JAK-STAT, PI3K, oxidative stress, cell death and heat shock response. Taken together, impaired ovarian function contributes to seasonal infertility that results from HS. This review paper describes physiological and endocrine systemic impacts of HS that may independently and collaboratively impair fertility in the porcine model. The review then details ovarian intracellular events that are altered during HS and finally determine futures needs in this area of research.

Optimization of thermal shock response spectrum as infrared thermography post-processing methodology using Latin hypercube sampling and analytical thermal N-layer model

In this work, we continue to develop and investigate the Thermal Shock Response Spectrum (TSRS) method as an alternative data processing method for infrared thermography (IRT). We focus on improving the current TSRS algorithm and present an optimization methodology for finding the optimal thermal Q-factor and characteristic frequency pair, which is based on the widely applied random sampling method. We show the qualitative relationship between the determined optimal characteristic frequency and the corresponding maximum difference in diffusion length between reference and defective models, as calculated by selecting a specific one-dimensional thermal N-layer model The investigations were performed on an inhomogeneous plate made of carbon fiber reinforced polymer (CFRP) with artificial square defects at different depths. Furthermore, two different heat sources were used: a xenon flash lamp and a laser. These sources are not only distinct by their underlying physics but also generate inherently different pulse shapes. To quantitatively estimate the contrast between defect and non-defect areas, and to compare these results with commonly used infrared thermography (IRT) data post-processing methods such as Pulse Phase Thermography (PPT) and Thermographic Signal Reconstruction (TSR), the Tanimoto criterion (TC) and signal-to-noise ratio (SNR) were used.

Immunometabolic Chaos in Septic Shock.

Septic shock is associated with over 40% mortality. The immune response in septic shock is tightly regulated by cellular metabolism and transitions from early hyper-inflammation to later hypo-inflammation. Patients are susceptible to secondary infections during hypo-inflammation. The magnitude of the metabolic dysregulation and the effect of plasma metabolites on the circulating immune cells in septic shock are not reported. We hypothesized that the accumulated plasma metabolites affect the immune response in septic shock during hypo-inflammation. Our study took a unique approach. Using peripheral blood from adult septic shock patients and healthy controls, we studied: 1. Whole blood stimulation ± E. Coli lipopolysaccharide (LPS: endotoxin) to analyze plasma TNF protein, and 2. Plasma metabolomic profile by Metabolon. Inc. 3. We exposed peripheral blood mononuclear cells (PBMCs) from healthy controls to commercially available carbohydrate, amino acid, and fatty acid metabolites and studied the response to LPS. We report that: 1. The whole blood stimulation of the healthy control group showed a significantly upregulated TNF protein, while the septic shock group remained endotoxin tolerant, a biomarker for hypo-inflammation. 2. A significant accumulation of carbohydrate, amino acid, fatty acid, ceramide, sphingomyelin, and TCA cycle pathway metabolites in septic shock plasma. 3. In vitro exposure to five metabolites repressed while two metabolites upregulated the inflammatory response of PBMCs to LPS. We conclude that the endotoxin-tolerant phenotype of septic shock is associated with a simultaneous accumulation of plasma metabolites from multiple metabolic pathways, and these metabolites fundamentally influence the immune response profile of circulating cells.